Why Low Vitamin D Isn't Actually Vitamin D Deficiency Problem
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"Vitamin D Deficiency"-Deconstructing the Deception by Jim Stephenson Jr
Fortification.
Sunlight, versus a dead lifeless photon-less pill. Did it begin this way????
Originally light was used to cure rickets, not Vitamin D. Vitamin D wasn’t even added initially to milk, the milk was irradiated or the cows were fed irradiated yeast.
“This initial fortification effort was followed in 1933 by the fortification of milk with vitamin D based on recommendations from similar groups. The addition of vitamin D to milk was originally accomplished by irradiating milk or by feeding the cows irradiated yeast. This technique was replaced in the 1940s by the simpler and more effective method of adding vitamin D concentrate to milk, as is currently practiced today (Quick and Murphy, 1982).”
https://www.ncbi.nlm.nih.gov/books/NBK208880
The vitamin D3 content is given for foods. Unfortunately (or fortunately) most of the foods that naturally contain D3 ALSO contain 25D, what everyone’s chasing. Funny it’s not included in the RDA ever and it should really make you question the goal even further. (Lots of folks are ingesting 25D directly and still struggling to hit the serum goal-that’s significant)
https://www.ncbi.nlm.nih.gov/m/pubmed/12743460/
https://www.ncbi.nlm.nih.gov/m/pubmed/24623845/?i=5&from=/12743460/related
Back to The Progression of stupidity. Once the Scientists were focused on “Vitamin D”, they worked feverishly to discover other analogs. Along the way they labeled any that failed to influence calcium inert. The ones that did, they would calculate their effectiveness compared to 1,25D to mobilize calcium. Read that last sentence again. If you are going to “mobilize calcium” let’s hope you do it from the gut and not the bone. This is where the hypercalcemia Axis comes into play and decides how much calcium and from where. Of course the where part depends on where it’s available as well. It may end up coming from bone and Osteoporosis may be the result. Sad thing is I haven’t run into people low in Calcium in my journey through the PANDEMIC DEFICIENCY where the main talking point is “It helps you absorb Calcium”.
“WHO’S LOW????” I ask.
Let’s think about the continuation of stupidity. Along the way it was discovered that tumors express Vitamin D Receptors (VDR’s). This is the “Era of Group Think Stupidity” we entered. This was after the 25D and 1,25D analogs were discovered in the late 60’s and early 70’s, as well as the VDR’s obviously. The tumor expression was viewed as a target for 1,25D, as if it were the tumors Achilles Heel. Actually, as if Cancer is stupid and sending 1,25D to those receptors will kill it. Stop and think about the expression of VDR’s. Your body will actually cease to express them to protect you but tumors express 300-400% more VDRs than healthy adjacent tissue. Where is the protection? It’s NOT in the tumor, that’s NOT YOU. That’s CANCER. The expression of VDR’s is a deliberate act. Try to get healthy tissue to express that many VDR. These are specific proteins made and folded in a very specific way, VDR’s. This is cancer WORKING, not sloppily leaving the back door open. They have a very short half-life, they are serving a purpose for the tumor.
What happens when they use 1,25D to target Cancer? The patients develop hypercalcemia and they all start talking about creating synthetic molecules that won’t lead to Hypercalcemia. This sounds EXACTLY like the molecules they labeled “Inert” and abandoned. (Where the steroid backbone is modified determines calcium influence, and this is known by the chemists.)
This is where I point out the dirty dogs circled back around and started to make similar molecules to the ones they had abandoned. This is the group that sought to exploit the VDR’s, the ones now failing via Group Think. There are other groups, and I will just mention one here because I will be writing about it in the future. There are the groups that sought to figure out what the abandoned inert molecules really were for and what they did. What a NOVEL idea. This is exactly what I would expect, but in the end this turns out to stay hidden and not be disseminated to the masses like it should have been. We are exploited by this group.
VDR Expression in tumor:
This should really make you pause and reflect. If tumors express VDR then hormone D can activate them. One thing it can do is encode the genes for the creation of macrophages. So macrophages can be created inside a tumor. STOP. Do you think having this occur is a good thing?
"One of the more prevalent immunosculpting outcomes of macrophages is increased aggressiveness (e.g. invasiveness, migration, growth, etc) of cancer cells. Several macrophage and tumor-derived molecules are implicated in the macrophage-induced augmented tumor aggression of which Wnt 5a is an example."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742305/
Now let’s look at some types of cancer where we know Vitamin D is anything but helpful. That is the purpose of this post.
Think of it like the “Ant Plant” Myrmecophyte, just not a symbiotic relationship. In this scenario the Ants are the cancer, the plant is us. The cancer uses our resources to grow and police itself using our immune system against us.
https://en.wikipedia.org/wiki/Myrmecophyte
Let’s look at Breast Cancer.
“The results showed that independent of ER status, breast cancer cells express the enzymes CYP24A1 and CYP27B1, which are responsible for converting 25(OH)D3 into its dihydroxylated forms. Moreover, these metabolites are produced at levels comparable to the levels observed in blood. They are positive for VDR, indicating that they can respond to 1α,25(OH)2D3, which can upregulate CYP24A1. These findings suggest that vitamin D metabolites may contribute to the tumorigenicity of breast cancer via autocrine and/or paracrine mechanisms.”
https://pubmed.ncbi.nlm.nih.gov/37244301/
Now let’s add a major worry for men as well, Prostate Cancer. What if you listen to the Mantra and got your 25D up there nice and high like they suggest for cancer??
“However, although VDR expression has a predominant role for vitamin D action, VDR may potentially function as an oncogene. “
“Loss of the vitamin D receptor in human breast and prostate cancers strongly induces cell apoptosis through downregulation of Wnt/β-catenin signaling.”
“Vitamin D co-regulates cell proliferation, differentiation and apoptosis in numerous tissues, including cancers. The known anti-proliferative and pro-apoptotic actions of the active metabolite of vitamin D, 1, 25-dihydroxy-vitamin D [1, 25 (OH) 2 D] are mediated through binding to the vitamin D receptor (VDR). Here, we report on the unexpected finding that stable knockdown of VDR expression in the human breast and prostate cancer cell lines, MDA-MB-231 and PC3, strongly induces cell apoptosis and inhibits cell proliferation in vitro. Implantation of these VDR knockdown cells into the mammary fat pad (MDA-MB-231), subcutaneously (PC3) or intra-tibially (both cell lines) in immune-incompetent nude mice resulted in reduced tumor growth associated with increased apoptosis and reduced cell proliferation compared with controls. These growth-retarding effects of VDR knockdown occur in the presence and absence of vitamin D and are independent of whether cells were grown in bone or soft tissues. Transcriptome analysis of VDR knockdown and non-target control cell lines demonstrated that loss of the VDR was associated with significant attenuation in the Wnt/β-catenin signaling pathway. In particular, cytoplasmic and nuclear β-catenin protein levels were reduced with a corresponding downregulation of downstream genes such as Axin2, Cyclin D1, interleukin-6 (IL-6), and IL-8. Stabilization of β-catenin using the GSK-3β inhibitor BIO partly reversed the growth-retarding effects of VDR knockdown. Our results indicate that the unliganded VDR possesses hitherto unknown functions to promote breast and prostate cancer growth, which appear to be operational not only within but also outside the bone environment. These novel functions contrast with the known anti-proliferative nuclear actions of the liganded VDR and may represent targets for new diagnostic and therapeutic approaches in breast and prostate cancer.”
Goes a long way to explaining the study below.
“In older men, lower plasma 25-hydroxyvitamin D is associated with reduced incidence of prostate, but not colorectal or lung cancer.”
“…every 10 nmol/l decrease in 25(OH)D concentration was associated with a 4% reduction in prostate cancer incidence (sub-hazard ratio [SHR] 0.96, 95% confidence interval [CI] 0.92–1.00). Every halving of 25(OH)D concentration was associated with a 21% reduction in incident prostate cancer in multivariate analysis (SHR 0.79, 95% CI 0.63–0.99). Following exclusion of prostate cancer cases diagnosed within 3 years of blood sampling, low 25(OH)D <50 nmol/l was associated with lower incident prostate cancer, and higher 25(OH)D >75 nmol/l was associated with higher incidence, when compared to the reference range 50–75 nmol/l, respectively (p = 0.027). Significant associations were also observed when 25(OH)D was modeled as a quantitative variable. No associations were observed between plasma 25(OH)D concentration with incidence of colorectal or lung cancer.
Conclusion
Lower levels of vitamin D may reduce prostate cancer risk in older men. By contrast, levels of vitamin D did not predict incidence of colorectal or lung cancers.”
https://www.sciencedirect.com/science/article/pii/S2211383518303526
https://www.nature.com/articles/boneres201723
https://journals.plos.org/plosone/article
Now let’s look at a cancer that is typically 100% fatal, Pancreatic Cancer.
“Higher vitamin D concentrations were associated with a 3-fold increased risk for pancreatic cancer (highest versus lowest quintile, >65.5 versus <32.0 nmol/L: OR, 2.92; 95% CI, 1.56-5.48, Ptrend = 0.001) that remained after excluding cases diagnosed early during follow-up.”
Circulating 25-hydroxyvitamin D and risk of pancreatic cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers
Clinically relevant 25(OH)D cutpoints were compared with a referent category of 50-<75 nmol/L. No significant associations were observed for participants with lower 25(OH)D status. However, a high 25(OH)D concentration (> or =100 nmol/L) was associated with a statistically significant 2-fold increase in pancreatic cancer risk overall (odds ratio = 2.12, 95% confidence interval: 1.23, 3.64). Given this result, recommendations to increase vitamin D concentrations in healthy persons for the prevention of cancer should be carefully considered.
https://pubmed.ncbi.nlm.nih.gov/20562185/
Careful what you believe.